Analysis of bcl-2, pten, p53 ve ki-67 expressions in endometrial cancer arising from endometrial polyp

Objective: The objective of this study was to compare the expression of the proliferation marker Ki-67, the antiapoptotic protein bcl-2 and the tumor suppressor genes p53 and PTEN between endometrium cancer arising from endometrial polyp and benign endometrial polyps. Methods: The study was performed retrospectively on 40 patients treated at Baskent University Hospital between 2006-2011. The patients who have been menopausal for at least one year were included in this study. The patients who have hormone replacement therapy, tamoxifen therapy or a history of breast cancer or who have not enough pathological specimen or who did not undergo full staging operation were excluded from study. Endometrial cancer developed from endometrial polyp was detected in %8 (26/323) of endometrial cancer cases. A total of 20 cases with endometrial cancer developed from endometrial polyp met the study criteria, and these cases were consecutively included in this study. Additionally, for each malign case, a random case with benign endometrial polyp diagnosed at hysterectomy specimen was included in the study. Results: The Ki-67 score was significantly higher in endometrial cancer arising from endometrial polyp group in comparison to the benign polyps (p<0,05). However, the bcl-2 expression was significantly lower in the endometrial cancer developed from endometrial polyp when compared to the benign polyps (p< 0,05). PTEN and p53 expressions were not different between the two groups (p>0,05). In patients with endometrial cancer, Ki-67, bcl-2, PTEN and p53 expressions did not differ among histological type, stage, grade, myometrial invasion, polyp size and lymphovascular space invasion with an exception of p53. p53 expression was significantly increased in higher grade tumors ( p<0,05). Conclusion: Based on the results of our study we believe that there is an inhibition of apoptosis and a decrease in proliferation in benign endometrial polyps. Possibly, at carcinogenesis step of endometrial cancer developed from benign polyp, other additional mutations cause a reverse effect and they increase proliferation and prevent the apoptosis inhibition. Key words: Endometrium cancer, polyp, p53, bcl-2, Ki-67, PTEN